The hazardous impact of a large number of xenobiotics in the environment, naturally occuring or man-made, is not well known. Risk assessment of such agents is complex because their biological effects depend, in part, on their metabolic activation and detoxification, and on their accessibility to target cells. Since chemical carcinogens are no exception to this generalization, we propose that environmental chemicals such as insecticides, other pesticides, drugs, food additives, and industrial contaminants may be risk factors in one or two ways. The first is that they are primary carcinogens or procarcinogens. The second is that they may be secondary risk factors or co-carcinogens because of their ability to modify the levels of metabolizing enzymes of environmentally abundant and established carcinogens. In this program, we propose to exploit fully the mouse embryo C3H 10T1/2 CL8 cells which have been shown to be sensitive to postconfluence inhibition of cell division for the detection of such primary and secondary risk factors among a selected number of insecticides, herbicide contaminants and fungicides.